Yannick Molgat-Seon1, Sabina A Guler2, Carli M Peters3, Dragoş M Vasilescu4, Joseph H Puyat5, Harvey O Coxson4, Christopher J Ryerson6, Jordan A Guenette7. 1. Centre for Heart Lung Innovation, St. Paul's Hospital, 166-1081 Burrard Street, Vancouver, British Columbia, V6Z 1Y6, Canada; Department of Physical Therapy, Faculty of Medicine, The University of British Columbia, 2177 Wesbrook Mall, Vancouver, British Columbia, V6T 1Z3, Canada. 2. Department of Pulmonary Medicine, University Hospital and University of Bern, Murtenstrasse 50, 3008, Bern, Switzerland. 3. School of Kinesiology, Faculty of Education, The University of British Columbia, 6081 University Boulevard, Vancouver, British Columbia, V6T 1Z1, Canada. 4. Centre for Heart Lung Innovation, St. Paul's Hospital, 166-1081 Burrard Street, Vancouver, British Columbia, V6Z 1Y6, Canada. 5. School of Population and Public Health, Faculty of Medicine, The University of British Columbia, 2206 East Mall, Vancouver, British Columbia, V6T 1Z3, Canada; Centre for Health Evaluation and Outcome Sciences, St. Paul's Hospital, 588-1081 Burrard Street, Vancouver, British Columbia, V6Z 1Y6, Canada. 6. Centre for Heart Lung Innovation, St. Paul's Hospital, 166-1081 Burrard Street, Vancouver, British Columbia, V6Z 1Y6, Canada; Division of Respiratory Medicine, Faculty of Medicine, The University of British Columbia, 2775 Laurel Street, Vancouver, British Columbia, V5Z 1M9, Canada. 7. Centre for Heart Lung Innovation, St. Paul's Hospital, 166-1081 Burrard Street, Vancouver, British Columbia, V6Z 1Y6, Canada; Department of Physical Therapy, Faculty of Medicine, The University of British Columbia, 2177 Wesbrook Mall, Vancouver, British Columbia, V6T 1Z3, Canada; School of Kinesiology, Faculty of Education, The University of British Columbia, 6081 University Boulevard, Vancouver, British Columbia, V6T 1Z1, Canada; Division of Respiratory Medicine, Faculty of Medicine, The University of British Columbia, 2775 Laurel Street, Vancouver, British Columbia, V5Z 1M9, Canada. Electronic address: jordan.guenette@hli.ubc.ca.
Abstract
RATIONALE: The pathophysiology of interstitial lung disease (ILD) impacts body composition, whereby ILD severity is linked to lower lean mass. OBJECTIVES: To determine i) if pectoralis muscle area (PMA) is a surrogate for whole-body lean mass in ILD, ii) whether PMA is associated with ILD severity, and iii) if the longitudinal change in PMA is associated with pulmonary function and mortality in ILD. METHODS: Patients with ILD (n = 164) were analyzed retrospectively. PMA was quantified from a chest computed tomography scan. Peripheral oxygen saturation (SpO2), 6-min walk distance (6MWD), and pulmonary function were obtained as part of routine clinical care. Dyspnea and quality of life were assessed using the UCSD Shortness of Breath Questionnaire and European Quality of Life 5 Dimensions questionnaire, respectively. RESULTS: PMA was associated with whole-body lean mass (p < 0.001). After adjusting for age, sex, height, body mass, and prednisone status, PMA was associated with %-predicted forced vital capacity (FVC), %-predicted diffusion capacity (DLCO), resting and exertional SpO2, and dyspnea (all p < 0.05), but not forced expiratory volume in 1 s (FEV1), FEV1/FVC, 6MWD, or quality of life (all p > 0.05). The annual negative PMA slope was associated with annual negative slopes in FVC, FEV1, and DLCO (all p < 0.05), but not FEV1/FVC (p = 0.46). Annual slope in PMA was associated with all-cause mortality (hazard ratio = -0.80, 95% CI:0.889-0.959; p < 0.001). CONCLUSION: In patients with ILD, PMA is a suitable surrogate for whole-body lean mass. A lower PMA is associated with indices of ILD severity, which supports the notion that ILD progression may involve sarcopenia.
RATIONALE: The pathophysiology of interstitial lung disease (ILD) impacts body composition, whereby ILD severity is linked to lower lean mass. OBJECTIVES: To determine i) if pectoralis muscle area (PMA) is a surrogate for whole-body lean mass in ILD, ii) whether PMA is associated with ILD severity, and iii) if the longitudinal change in PMA is associated with pulmonary function and mortality in ILD. METHODS: Patients with ILD (n = 164) were analyzed retrospectively. PMA was quantified from a chest computed tomography scan. Peripheral oxygen saturation (SpO2), 6-min walk distance (6MWD), and pulmonary function were obtained as part of routine clinical care. Dyspnea and quality of life were assessed using the UCSD Shortness of Breath Questionnaire and European Quality of Life 5 Dimensions questionnaire, respectively. RESULTS: PMA was associated with whole-body lean mass (p < 0.001). After adjusting for age, sex, height, body mass, and prednisone status, PMA was associated with %-predicted forced vital capacity (FVC), %-predicted diffusion capacity (DLCO), resting and exertional SpO2, and dyspnea (all p < 0.05), but not forced expiratory volume in 1 s (FEV1), FEV1/FVC, 6MWD, or quality of life (all p > 0.05). The annual negative PMA slope was associated with annual negative slopes in FVC, FEV1, and DLCO (all p < 0.05), but not FEV1/FVC (p = 0.46). Annual slope in PMA was associated with all-cause mortality (hazard ratio = -0.80, 95% CI:0.889-0.959; p < 0.001). CONCLUSION: In patients with ILD, PMA is a suitable surrogate for whole-body lean mass. A lower PMA is associated with indices of ILD severity, which supports the notion that ILD progression may involve sarcopenia.
Authors: Renata G Mendes; Viviane Castello-Simões; Renata Trimer; Adriana S Garcia-Araújo; Andrea Lucia Gonçalves Da Silva; Snehil Dixit; Valéria Amorim Pires Di Lorenzo; Bruno Archiza; Audrey Borghi-Silva Journal: Front Rehabil Sci Date: 2021-11-16